Treatment of the receptor-positive breast cancer cells (BT474 and MCF7) with rapamycin resulted in a rapid inactivation of the mTOR downstream molecule p70S6K, evidenced by a decrease in phospho-p70S6K at Thr389, and a substantial reduction of oxygen consumption, suggesting that the mTOR/p70S6K pathway was important for maintaining mitochondrial respiration in these breast cancer cells (Figure 3A, B). This evidence concerns the gene RPS6KB1 and breast carcinoma.